tv Charlie Rose PBS February 23, 2012 11:00pm-12:00am PST
>> rose: welcome to our program. tonight a special edition of the charlie rose brain series year two. in the fourth episode we consider alzheimer's disease and temporal dementia. >> it's helpful t divide it with age into two categories. it's called age-related memory loss, normal aging or forgetfulness and the dementias. now, the dementia that is most common is alzheimer's disease. what do we understand about these diseases. are there genes identified that are important are there little
genes or bigger genes with larger effect? we also want to understand how do we approach these this in terms of treatment >> rose: episode four of the charlie rose, episode four coming up. the charlie rose brain series is the most exciting study of our time studies about the brain and the mission is to advance the frontiers of research in the basic sciences and mathmatics. funding was provided by the following:
alzheimers disease is loss of memory and temporal di temporale diseases that take a toll on those diagnosed and everyone around them. patients are robbed of their independence, their relationships and their very identities. alzheimers is the most common degenre t bra disease. today more than 5 million americans have it and predicted by 2050 there will be three times as many cases. f.t.d. is often misdiagnosed as alzheimers and the effects are just as devastating they're a cluster of diseases that control behavior, language and decision making. some people undergo dramatic changes in their personality and others lose their ability to use and understand language. remarkably some patientsith
f.t.d. can experience burst of creativity when other regions take over. at the moment there is no cure or effective way to slow it progression of alzheimers or frontal temporal dementia but research has brought research to the diagnosis and the pathogenesis and treatment. after the program was recorded a few weeks ago, two independent studies conducted by columbia and harvrd shed light on the disease and it can spread from brain cell to brain cell like an infection. dr. scott small is a coauthor of the study and appeared february 3 to talk about the developments. >> early stage of alzheimers the patien patient dies and you find it in area a and you see alzheimers in two areas and then three areas and that's always been known for the last 20 years. and the question has aays been
does area a juto b and c or are they just different areas that are vulnerable and pop in at different time points. that's a very difficult question to answer with human patients. what we did at columbia and brad hyman at harvard we used genetic engineering to introduce the pathology of alzheimers of area an in a mouse and that's the pathway. the pathway begins in the area called e interonal cortex and it's starts in the hypocampus and spread and that might account for why when we do follow patients with alzheimers it begins with mild forgetfulness but as it progresses you get language problems, etcetera. >> rose: how does it go from one cell and region to another.
>> we don't know that. we have theorys. the big news is we showed it does. in other words, i wasn't clear th it d and now that has this has been shown it becomes an incredibly difficult question. >> rose: as i noted the new york times earlier of the new developments on alzheimers and my interview with dr. small came after the program you're about to see. we show you this remarkable group of scientists to talk about where we are in understanding and fighting the diseases. mark tessier-lavigne heads the laboratory of brain development and repair. and alison goate was professor at washington university in st. louis school of medicine. david m. holtzman is a jones professor and chair of neurology in st. louis and an eric kandel.
he is as you know a nobel laureate and tells us what it is we're about to see d talk about. >> we're full of stories about alzheimers. many people have been touched about it, their parents, grandparents. we know also that there's something called age-related memory loss. help me understand what we want to do discover in this conversation. >> as you pointed out, it's very helpful to divide memory loss with age into two categories. what is called age-related memory loss, normal agi or benign fortfulss and dim end has. it's part of the normal aging process. just like your muscles might get weaker if you don't exercise
them a lot you get stiffer. so there is a weakening with age. this is contrast to dementia which is a progressive much more serious disease and has impact in other aspects in memory storae. with normal aging there's good news as you'll hear from david holtzman there are ways to counter active. running two television programs the same day as what we're doing. >> rose: that's why i did it, see. exactly the reason. it wasn't the money or the opportunity, it wasn't ambition, it was counter act. >> that's the way to do it. >> rose: you once said to me find new ways to use your brain that have not been challenged before and this is benefit. >> this is dogit. >> rose: for all the people who say i'morkioo hard, te at.
>> this -- so this is very good news. in contrast dementia for which we have no cure as you point the out is an epidemic. there are 5 million people that suffer from it by now and by age they're three to four percent of people age 70 have dementia. age 80, it's 20% and age 90, 50%. it's just horrible. now, the dementia most common is alzheimers disease. in 1906, it was described a case he said was unlike anything he'd ever seen. there was a woman with memory loss and peculiar thoughts and thought in almost an irrational
way her husband was complicated and she was getting jealous of about what he was doing. as time got on she became suspicious of other people as well. she thought they were out to get her and her memory deteriorated more and found difficulty getting around her house and after a while had to be hospitalized and then after five years of hospitalization she died. when she was autopsied, alzheimers did the autopsy and found three features davidnd alison will describe. there's a shrinkage of the brain, the cerebral cortex and plaque outside the nerve cell and tangles within the nerve cell. many people think this is the only dementia, as you pointed out, there are a number of other
dementias, vascular dementia and a decade before heim described it frontal temporal dementia and it's a fantastically interesting disease because it involves at least at the beginning very selective regions. so in addition to memory loss if you have damage to the frontal lobe as you indicated you have a disinhibition. people who never drank before will start and those who never gambled before will start to gamble. if it spread back to the temporal back and other areas get involvementof langua as well. there are a number of things you want to know about this which particularly allison will have a lot to say and that is what do we understand about these diseases. are there genes that have been
identified or small genes or larger genes with larger effect? we also want to understand how do we approach these things in terms of treatment and we're fortunate with marc here who is noonly an outstanding scientist but gentech has experience of how to bring drugs to mark it and can explain to us why it's so difficult to bring a drug to market and extraordinary expensive. we'll learn an enormous amount. >> rose: let's start with david holtzman and talk about the difference between age-related and alzheimers and the difference between early onset alzheimers and late onset. >> all right, so a frequent question i often get from family members and patient is wh's the difference between dementia and alzheimers disease and dim en
dementia is impairment and alzheimers causes dementia. the other common causes are strokes, a parkinson like symptom and frontal the frontalo somtimes when it's changes it's difficult to tell and people have trouble with names, have slowing of think. a little trouble with memory but what's not normal is for someone to begin repeating themselves, to forget conversations, to have trouble with your checkbook when you never had trouble before. those are signs something is wrong beyond normal aging. >> you made an interesting point. if you worry about your memory loss you are unlikely to have alzheimers disease because you have the insight there's something wrong with your memory. >> a lot of people really worry
about their memory and people who are worried don't get it and the ones that don't don't realize they have a problem. >> rose: there's a mel goods video. >> so mel goods was the former ceo of warner lambert and gives insight in a poignant way of what's it's like getting alzheimers disea and might b worth watching. >> rose: let's watch the video. >> what do you do when you talk to your doctor and you're doctor says the following: the only words you don't want to hear, i'm sorry, you have early stage alzheimers. not long ago nancy and i had to confront this reality. i recommend my first
reaction, "but doc, i feel fine. in fact i feel great." my first thought was," i'll beat this." and i had a good record of beating the odds. at 30 i became the youngest manager and art a string of leadership jobs i was asked to run the company. in 1991 i became chairman of warner lambert. we went from a company with praccally nothing in the pipeline to the enterprise then invented what is now the world's best-selling medicine li medici. remembering all the times i faced long odds and didn't blink, i wondered why can't i beat alzheimers too and then over a few days the reality set
in. alzheimers disease is pitching a perfect game. i don't expect bio medical cien to rideomy rescue but i will go out a happy man if we can change the course of this disease for the hundreds of millions of people who will soon be at risk. >> rose: so what should we take from that? it's a powerful lesson his eloquent testimony is as of now alzheimers will win. >> i really think the amount of discoveries that the field has made over the last 30, 35 years really give us hope we will eventually conu! eventuall eventually conquer this and he described these legions
we talked about and the plaque and you the amoloid plaque and the next arrow you see a neuro fiblarry single. ey were we now know they're fundamentally involved in the cause of the disease which we'll talk about more as we go along. >> it gives us hope if we can detect them as they're occurring we may be able to prevent the damage to the brain. you can see these lesions, these ammo loid plaque attack certain
regions and they build up in the prefrontal cortex involved in problem-solving and the fronta prior cortex and there's a reserve the brain has so people seem fine for a while. you can't tll the difference between someone who has the lesions initially and not but after time as more and more damage builds up in the brain you can see the brain begins to shrink because the nerve cells and their connections are being lost and damaged and regions like the hyphypocampus gets sma and that's what a pathologist sees under a microscope and now see them with imagei but what we've learned over the last 25
years is the underlying science about the disease and while we don't know everything we have a lot of insights the field has made. for example, this amoloid protein which accumulates in the brain of people with alzheimers disease is shown in red. we know it's derived from the amoloid precurser membrane and science went in to figure out how the red part of that gure gets separated from the protein and it was figured out there's enzymes, one called beta and the gamma cut that the enzymes clean it the larger protein and forms the amoloid protein and this a beta is made by all of us all the til time a normal product m by our brains and what happens
inlzheimers is e soluble ptein clumps up and forms aggregates and when they form there's evidence they can become toxic to cells and that's one -- that's a major theory that appears to be the case and once this starts happening not only can it damage the cell directly another protein can also normally soluble can begin to clump and they appear to play an important part in the progression of the disease. >> rose: let's talk about the genetic consideration here. >> it looks like a single pathway of disease. the genes at the top there the protein which david mentioned,
people can have mutations in the genes that cause the deasend wh w uerstandtthe mutations lead to increased production of that a beta fragment. it seems fob the earliest change we can find in the people to pinpoint the amoloid protein to be central to the disease. >> rose: where was the focus of the genetic research? >> right now most of the research is on understding risk factors for the rest of the cases the 99.9% of cases. >> and causedbury a single gene defect. >> caused by many genes of small
effect and also environmental factor may play influences an other morbidities and the findings have pointed to e amoloid thway. whatever is the proximal cause of disease it all filters into the same pathway that affectsing araigation of the amoloid peptide and loss of cells and dementia. >> we don't know for certain whether it's the ultimate truth as you pointed out but it's a very powerful hypothesis that's been extremely useful in research and very reassuring because in other diseases we'll discuss like schizophrenia and depression you can't point to a single gene that can do it for so so it's lots of little genes that seem to be responsible and
to figure out how those diseases work is of the more difficult so though the progress at the moment seems to be very slow our understanding of it has been really amazingly rapid. >> so we were able to make animal models in fact of the disease by taking these very genes and mutations and introducing them into a mouse andbefe that there was no animal laboratory model. >> rose: what what happens? >> that's mouse ages there are changes in the brain that change in the protein you see in humans and in some of the mouse models there is some suggestion there may also be some changes in memory in these animals. it'sot a perfect reprentaon of the disease.
>> the representation is that mouse only lives to be two years old. while alzheimers you don't even see anything for years. with you have to suspect the disease is going on. there is cognitive deficits and it's very encouraging. >> rose: let's talk about the differences between alzheimers and frontal temporal dementia. >> most have never heard of frontal temporal dementia and that's because we didn't know about it until recently even the neurology textbooks said don't pick disease because they thought it was so rare and they thought we couldn't separate it during life from alzheimers disease. we've learned people under the
age of 64 it changes ase get over 65 and as allison will talk about we know about the genes that cause, there are different genes and protein thattin that n the brain. if it starts onhe left side starts in speech anduddey spech is affected but often what you see is a profound idea of people >> we found about half of our patients early in the illness
either were arrested or could have been arrested for something that they did associated with this new illness. other fasnati things about th disse is it hsthe part of the brain that allow us to relate to others to sympathize and empathize with other people. >> rose: the right side. >> that's the right side, absolutely. so you see these people who were once loving who become cold and different to people around them. they become addictive and overeat and smoke when they never smoked before. this is a profound social disorder that has a huge impact on a family. it hits people when they're younger so these are often pele ware working at a critical point in their life. i would say often if not always we see people make bad judgments around their finances. sometimes they become bankrupt, often become alienated from
their loved ones. >> rose: are there specific genes that contribute? >> it offers great hope for treatment. >> rose: tell me about the genetic competition of f.t.d. >> we discovered in contrast to alzimerdisese wre so far all the evidence pointed to a single common pathway, what we've discovered about frontal temporal dementia is it's many diseases as you can see we've actually identified. three different genes and they cause a similar clinical disease but the pathology will look different and the genes that are altered are different so we have parallel path ways where you have similar looking disease but different underlying causes and it has i a implications for
treatment and with alzheimers if you can modify the central pathway that appears to be present in all these diseases you might be successful with the treatment targeting that whereas in frontal temporal dementia it's probabl probably multiple and we'll need to understand which form an indivual has before thinking about treatment because the treatment could be different. >> rose: before we go further, tell me definition of dementia. >> dementia is a loss of memory in cognitive function with an emphasis. >> rose: so loss of memory in a cognitive function. >> more than memory. as spects of cognition. >> it needs to interfere with our social and occupational function. it has to affect your daily life. >> rose: okay. let's move to where you are in terms of basic sciences and
looking at discovery of marketable and safe products. >> maybe i can talk in the progress of drugs for alzheimers and later maybe we can come back to frontal temporal dim en deme. there are a few drug approved but that's a modest benefit and boost the number of cells that remain and help in terms of brain function but is temporary because they don't target the underlyin underlying the brain continues to deteriorate but they don't make a big dent in the disease and we need drugs that slow or block the progression of the disease by targeting the underlying mechanism. now unfortunately several drugs that attempted to do that are been failed and what many are pinning their hopes on are ones
that center on the amoloid protein and the beta peptide that forms plaque and a beta are bad actor has it drive the disease and have to be stopped. now it's taken a long time to develop drugs for the target a beta. the drug discovery is inherently a lengthy and costly and risky business but on average it takes 14 or 15 years and about a billion dollars to make drug and the attrition is just massive. so when you start to make candidates nine turn out to be safe enough to enter human clinical trial and only one of nine will make it all the way through to approval with the
others failing either because they proved to be unsafe or because they just don't work. in the case of alzheimers disease there's a further hurdle which is there's prective barrier to keep drugs from entering the brain and it's difficult. a beta was discovered over two decades ago and it took a decade for people to figure out an approach to get access to a beta in the brain and applying that approach they're now half a dozen drugs some in late-stage clinical trials and some are shown to reduce the plaque in the brain of alzheimers patients and in this calendar year in 2012 we should see the clinical results wh one of them and others giving results in subsequent years. >> rose: if the trials are satisfactory what is the result >> the result is a slowing of cognitive decline. >> rose: so it's not you can reduce the impact of the erosion
or destruction. >> it's due to loss of cells. there is limited regeneration of nerve cells but not in most regis otherain but excuse me, there's another hopeful sign we should mention before and there's a combination of new insights into how to interven interven intervene therapeuticly and -- >> that's a very important point. one of the biggest concerns with the ongoing trails is they're in pience th are asymptomatic and many are arguing we should be doing the trials in people that are presymptomatic based on
new markers to detect the disease before the symptoms appear and david is a world expert on this and maybe can comment on it. >> that's like cardiovascular disease. we know the plaque has it build up in the heart that block the arteries take years to build up and some of the most eventative treatments are to get your cholesterol checked and we have markers that tell us they're occurring in the brain while they're cognitively okay. some are imageing and some are checking the fluid or blood and what's work the best is spinal fluid. we can tell someone is likely going to develop alzheimers disease in the next few years and if things like that are applied in clinical trials maybe we'l we'll beble to delay or
prevent the disease. >> rose: so maybe you'll see it into five or ten years into development. >> that's exactly right. there's good evidence we can do that now. you enroll people of a certain age and assess the biomarkers and put them on a treatment or placebond it takes many years for it to progress. it's going to be very expensive to do the trials and how even a single pharmaceutical company it may be difficult and we may need to come up with new models maybe public-private partnerships or new ways to enable us to get a treatment but i think that's the way to go. >> or find surrogate markers so you go early before symptoms appear and give the drug and you
measure outcome not based on the velopmentf alzheims disease per se but some further progression, pre-symptomatic condition. >> like cholesterol, if you take a drug and it gets lower this could occur in alzheimers disease. >> rose: let's move it over to where you are. >> the frontal temporal dementia has given us incredible genes and people of five percent carry the gene that produces sething calle we don't get enough from the bad gene. it becomes one of the most plausible areas to treat something. all you have to do is figure out a drug that will either increase the amount of pro granulin in the brain or deliver the protein and becomes one of the simplist
diseases and beginning trials with things we think will elevate the progranulin levels thebrain. >> rose: talk about the creativity in the left side of damage there and what that tells us? >> yes. so 1996 i started to notice that some of my patient all had progressive e progress ephasia and began to show visual creatity and it tel uswe hve circuits and we turn one off and may actually be turning other circuits on and in some of these patience there's increased activity in the posterior parts of the brain
that is involved in creating art and ann adams -- >> rose: i love this story. >> ann and her husband both scientists, he was a mathmatician and ann was a biologist thattudied the epithelium of the ovary under the cell and her workability and it became more visually beautiful. >> rose: the became obsessive. she just wanted to go to the art studio and just that was her life. >> exactly. >> rose: so a scientist that becomes moreommitted to art than she could eve have imagined. >> her whole life became art and painting. >> rose: because it moved to a different section of the brain. >> we got a picture of ann's
brain before she ever developed her language disorder and saw already she was showing loss of tissue and had loss of tissue initially in the left part of the brain involved with producing speech and a larger right posterior parietal area and that was the beginning of the frontal temporal dementia. i wanted to talk about the picture of ann's which she said unraveled bow unraveled bollero and attempted to capture what bolerro does and it's a rhythmic, repetitive compulsive piece similar to the way anna approached the art. >> rose: note by note. >> she took this 340 meter piece with a progressive crescendo and
began initially with the begins of this and showed in a snakey fashion how the crescendo builds if the note is longer it means that bolerro was producing a louder note, if it was wider they played the note longer and what you see is the sudden change in key which ann adams was fascinated by. so suddenly we've gone from these dull blue and blue keys to this gaudy florescent pink and orange which is the beginning of the crescendo and the stop of the music. and so ann had done something we called transmodal association. he associated sound, rhythm, o d
auditor auditory combinations. >> we don't think it's a coincidence that revel himself was beginning to have problems with writing and developed the same progressive ephasia like ann's and neither knew about the other. >> rose: let me tie up the idea of the genetic disorder with environmental impact. >> right, so, the well described example of how environment can play a role relates to the most common risk factor for
alzheimers disease which is particular perform of a protein called protein e or apo e for short and it comes in three forms and two, three and four, bizarrely not one and the three is the most common form and it's neutral in terms of risk. the apo 4 increases our risk for developing the disease and 2 decreases one's risk for alzheimers disease and what's been observed is if you have head injury with loss of consciousness, if you have an e-4 form theft protein your outcome is much worse than if you have one of the other forms
of the protein so this is an example of where an environmental factor, head injury, can have a different impact on your risk for disease depending on your underlying genes. it's rally quite substantial increase in risk so people who have the apo e-4 of the protein and have a head injury can have a 15 to 20-fold increase in risk in developing alzheimers disease. this has a big impact when you think about the sports that people play where you've contact sports -- >> rose: concussions seeming to be on the rise. >> that's right. i think it has significant public health issues with people putting themselves at risk for
developing alzheimers disease or other dementias as a result. >> rose: before i open it up to broader questions. talk to me about drugs and what we learned in the sense if in fact the drug fails does not mean they're not les lessons to learned. >> we di discussed the ongoing trials against the peptide is it because the theory was incorrect or intervened too late and the horse left the barn and closing the door won't keep it in and the trials will see effects on amoloid or whether there's behavioral improvement and in cognition and able to learn how good our theory is and that's one thing that will happen over the next several years. at the same time, as we target one specific mecnism the it's important we continue to target other mechanisms.
one of the great lessons of drug discovery is you can get a magic bullet. typically you need combination of drugs and an very important area in nerve degeneration is understanding once the disease is initiated with factors like probeta and progranulin what are the executioners of the nerve cell death. it's thought the tau protein is involved in this and drugs against tau are being made and developed and they can work in a complementary fashion. >> rose: when we look at the concentration of tao what do we see? >> we see it increasing in spinal fluid over time. tao is interesting because it's in the tangles david talked
about the neury fib you'llr >> the execution pathway may be where you can get a drug that works across dim en dementias. >> rose: let's broaden this out and talk when the cost. there's huge societal cost. >> ormous. >> one forgets and this is one of the things that marc pointed out, the costs are true for cancer as well. it takes a long time to bring a drug to market. the reason the cost is so enormous here is because there's an epidemic and so much population is suffering. as a medical student this was
not talked about. this is a dramatic increase. >> rose: when you were a medical sdent tre was no discussion alzheimers. >> practically not. >> me neither. >> interesting in terms of societal cost currently the alzheimers association reports that the cost to society today in the united states alone is about $280 billion a year and that's where money changes hands primarily through nursing care and it doesn't involve in-kind care of families and there there be a tripng in 50 years and the cost will be a trillion dollars a year. it shows you the magnitude of the economic impact and not to mention the human toll. >> the country's beginning to
realize there needs to be an effort and the government plans that by certain dates hopefully there will be significant progress on this. >> rose: a great question is the cost of health care as a percentage of g.d.p. and how it make a more effective and more efficient health care treatment. and delivery of health care. >> right. what's fascinating is that first he reminds me of president ragan who also came public with it realizing it's not going to do much him perhaps but people will know what an important disease it is. mel goods company is the first company trying to develop a drug for alzheimers disease. >> rose: i alwayshought that ragan's decision and the eloquence he said about alzheimers and the way he said it was one of the significant
contributions he made. >> absolutely. >> taking the stigma away from the disease. it's not bad behavior. >> we had a spokesperson at that time and we don't have a spokesperson at theoment for alheims disease and suddenly we have these incredibly powerful biological approaches and we're not getting the n.i.h. funding. >> rose: so you're worried there's opportunity that we may miss the chance to activate. >> exactly. >> we finally have the discoveries now we have to act and get treatments that are effective. >> rose: and the need is so large that primarily government can provide the resoues necessary. >> more than that as well.
>> the government has to be involved it's of such large size and what is tragic is with the cutback in government spending, research is being hit particularly hard. we are fortunate that the people like the lauders are interested in the alzheimers deed and it's a private thril philanthropy. >> rose: we hear all the time we should all be doing thgs to make our brain more activity. i'm not sure i understand what is the hard empirical evidence of doing that. >> if you keep your mind active and actually being in good health, keeping blood pressure under control and diabetes, these are protective factors against age-related memory loss. that's something we can actively do something about. >> rose: as we've made very
clear here and everyone knows that more and more you meet people that have in some way been connected to either some kind of dementia or alzheimers itself. we are where here in terms of the research and the possible breakthroughs in the near term? >> i think we understand a lot, not everything about what underlies the deed and we are at a point where new treatments being developed now are in people for the first time that really attack the mechanism and we're probably also going to have to to treat earlier and the'sope to delay the disease or prevent in the next 10, 15 years. some of the markers are being abl abl able to image amoloid and in the spinal fluid detect whether the brain is beginning to degenerate
by marking tao and you can detect roughly when somebody's likely going to develop the disease. >> i think it's worth pointing out thathe progress habeen exciting in terms of the basic science and working towards the clinic with the experimental drugs and there are still many things we don't know for example, how the nerve cells are dying which if we knew it would enable the next generation of drugs so while we move forward with the new drugs in the clinic we have to keep at it. >> rose: we don't know where the nerve cells are dying? >> they're dying because of the triggers whether it's progranulin or a beta. we don't know how the nerve cells get dismantled. what's the program of suicide at the biochemmic level. >> rose: how far away do you
think we are of that? >> i never make predictions in signs but i think we're poised to make a lot of progress in the coming years because insight how to how cells die have arisen in the last two decades converging on understanding a nerve cel >>hemakes a good point which we've made repeatedly here. the brain a marvelous organ and we like to think we understand it but we're far from doing that and this is more true in terms of treatment. these are extremely difficult problems and it's going to take a long time to really tackle they will and one has to realize molecula molecular imageing techniques with the most primitive techniques of visualizing and you didn't visualize the brain but the vascular and others in
30 years. >> rose: i'm struck no matter how sophisticated the sign and biochemistry, no matter what it is, it's always ripe with basic fundamentals unless you understand why the nerve cells are doing that you can't go to understand how to address the issue. so let me do something we always do here and with interesting results and me may have been on it with you but what's the most important question you'd like to see answered? >> how it is the nerve cells die in these diseases. >> i want to know if you treat the disease with these attractive mechanism-based therapies could prevent it. >> rose: and you're optimistic. >> i think in the next 10 to 20
years. >> i spent 30 years working on diagnosis and the i don't want to work on that i think we're good at it now i want to spend the rest of my time proving we can treat frontal temporal dementia. i think it will be like cancer. we won't treat all cancer at the same time. we'll pick off different sub types, alzheimers disease, one by one and with progranulin and the tao related problems of f.t.d. i think we're make headway. >> yes, i would agree with dave and i think that maybe a combination of knowing our genetic background and genetic respecters in combination with the markers will allow us to identify people who are at most risk at the earliest possible times to allow these treatments to be used to prevent disease rather than to be curing the disease. >> rose: memory is your game.
>> i have nothing to contribute to these people my thi is memory. what i like is bruce's finding that there's an increased in creativity because there's an idea that one of the founders of neurology is the left hemisphere inhibits the right hemisphere, if you remove the in hibition emerges and we've seen it with various diseases release certain plasticities. thank you, thank you.